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Clinical & Experimental Allergy

Increases in collagen type I synthesis in asthma: the role of eosinophils and transforming growth factor-bβ

Authors

  • A. Nomura,

    1. Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
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  • Y. Uchida,

    1. Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
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  • T. Sakamoto,

    1. Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
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  • Y. Ishii,

    1. Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
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  • K. Masuyama,

    1. Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
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  • Y. Morishima,

    1. Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
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  • K. Hirano,

    1. Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
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  • K. Sekizawa

    Corresponding author
    1. Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
      Kiyohisa Sekizawa, Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennoudai Tsukuba, Ibaraki, 305–8575, Japan. E-mail: kiyo-se@md.tsukuba.ac.jp
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Kiyohisa Sekizawa, Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennoudai Tsukuba, Ibaraki, 305–8575, Japan. E-mail: kiyo-se@md.tsukuba.ac.jp

Summary

Background Collagen type I is one of the major deposits in thickening of the reticular basement membrane of asthma.

Objective and Methods In this study, we assessed turnover of collagen type I in asthma by measuring procollagen type I C-terminal peptide (PICP) and collagen type I C-terminal telopeptide (ICTP) in induced sputum.

Results PICP but not ICTP was found to be significantly higher in asthma subjects than in normal volunteers (P < 0.05). In asthma, PICP was inversely correlated with %FEV1.0 (r = −0.539), and its levels significantly increased upon exacerbation (P < 0.05), indicating that collagen synthesis increases during asthma exacerbation. Additionally, PICP was found to significantly correlate with eosinophil counts in sputum (r = 0.539), indicating that eosinophils stimulate collagen turnover. Because eosinophils can produce TGF-β, a potent stimulator of collagen synthesis, we immunocytochemically examined TGF-β-positive cells in sputum. TGF-β-positive cells significantly correlated with eosinophil counts (r = 0.811) and PICP (r = 0.569), suggesting that TGF-β released from eosinophils is involved in collagen synthesis.

Conclusions The results of the present study suggest that collagen synthesis is stimulated in asthmatic airways by eosinophils through TGF-β, while collagen degradation is not, and that PICP in sputum can act as a new marker for airway inflammation in asthma.

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